Your Appetite is Controlled by Your Genes

Dieting is a culturally acceptable way of controlling our appetite and limiting weight gain. Whether diets suppress our appetite by making us feel ‘fuller for longer’ or simply reduce our caloric intake, not all people need them to control their weight. Why is this? Why is it that some people struggle more than others to lose weight? Could this be genetic?

As it turns out, genetics do seem to play a role. Perhaps surprisingly however, they have a larger influence on our appetite than our metabolism. People who gain weight faster seem to do so as they feel hungrier more often than those who are naturally thin.

A study from the University of Cambridge comprising of DNA samples and medical records of over half a million people aged between 40 and 69 years old has identified a gene, MC4R, as being responsible for our appetite.

Normally, after we eat a meal, the MC4R gene is switched on to signal that we are full. Once we have stopped eating and feel satiated, the gene is turned off. However, it does not always work. As many as 300 mutations of the gene have been found.

These mutations are the most common single-gene cause of obesity, accounting for 6% of children with severe obesity. Unlike those with a normally functioning MC4R gene, those with certain mutations never receive the signal that they are full. This means that they always feel hungry and are more likely to overeat, and thus gain weight.

Alternatively, however, some mutations of the gene mean that it is constantly switched on. Affecting around 6% of the population, this may explain why some are naturally thinner - they simply don’t feel hungry due to the constant activation of the MC4R gene creating a feeling of continual satisfaction.

Dr Sadaf Farooqi, who led the research into the gene has said that this information proves that MC4R is an important controller of weight, and that the new pathway it reveals is now an obvious target for drugs fighting against obesity.

To conclude, the MC4R gene has been identified as a key indicator of how our appetites function. With over 300 mutations, its improper functioning may lead to a feeling of constant hunger leading to obesity, as well as constant satiation leading to a higher likelihood of being thin. Its discovery means that further research needs to be conducted in regard to the gene as a possibility for fighting obesity in the future.